(4) Z lines – the ends of the sarcomeres, where the actin ends are attached

C. SLIDING FILAMENT MODEL OF MUSCLE CONTRACTION

1. There are head and tails to myosin; the heads (like golf clubs) attach to binding sites on the actin; contraction occurs when they are released, bind to a further binding site, then rest and contract

4. T-tubules – deep invaginations in the cell membrane to help with depolarizing the entire cell

F. MECHANICS OF CONTRACTION

1. Force of contraction can be increased in 2 ways:

a) Motor unit recruitment: one motor neuron innervates multiple myfibers; a twitch is the smallest activity, is the activation of only 1 cell; a larger twitch or contraction can be activated by recruiting the rest of the cells in the motor unit

b) Frequency of summation: repeatedly stimulating the motor unit between impulses (after refractory period but before Ca++ is resequestered in sarcolemma) will results in a stronger contraction (maxing out at tetanus)

2. Length-tension relationship – muscle fiber contracts the most strongly at a specific length, where there is max overlap between actin and myosin (2.2 microns)

III. 10.3: CARDIAC MUSCLE COMPARED TO SKELETAL MUSCLE

A. SIMILARITIES

1. Thick and thin filaments are organized into sarcomeres; both are striated

2. T-tubules are present in both

3. Troponin-tropomyosin regulates contraction in the same way

4. The length-tension relationship works the same way and it is more significant in cardiac muscles

B. DIFFERENCES

1. Cardiac muscles are not structurally syncytial (each only have 1 nucleus) while skeletal muscles are syncytials

2. Cardiac muscle cells are connected by gap junctions known as intercalated disks which allow the action potential to propagate throughout the entire heart without sharing nuclei or cytoplasmic contents (functional syncytium)

3. Connected to several neighbors by intercalated disks (branching?)

4. Cardiac contraction does not depend on stimulation by motor neurons (stimulation by ACh is actually inhibitory

7. AP depends on location of smooth muscle cell; can elicit spike potentials (above threshold), but it is more difficult because there are no fast Na+ channels, only slow; takes much longer to propagate AP than in skeletal muscle

8. Smooth muscle can sustain prolonged contraction

9. Have constantly fluctuating resting potential (slow waves); when RP decreases and a spike potential occurs, this is when an AP gets propagated (ACh is released in response to local stimuli to cause the spike potential; NE inhibits amplitude of slow waves

10. Innervated by autonomic motor neurons

Feature

Skeletal muscle

Cardiac muscle

Smooth muscle

Appearance

Striated

Straited

No stration

Upstroke of AP

Inward Na+ current

Inward Ca++ (SA node)Inward Na+ (elsewhere)

Inward Na+

Plateau

No

Yes

No

Duration of AP

2-3 msec

150 msec (SA node)300 msec (other cells)

20 msec

Ca++ from

voltage gated Ca++ channels, Ca++ from SR

voltage gated Ca++ channels, inward Ca++ during plateau, Ca++ from SR

voltage gated Ca++ in membrane

Molecular basis for contraction

Ca++ troponin binding

Ca++ troponin binding

Ca++ calmodulin binding, MLCK activation

Fuctional syncytium

No

Yes

Yes

Contraction dependent on extracellular Ca++

No

Partially

Yes

V. 10.5: OVERVIEW OF THE SKELETAL SYSTEM

A. Axial skeleton – skull, vertebral column, ribcage

B. Appendicular skeleton – the remainder (including the pelvis, but not the sacrum)

VI. 10.6: CONNECTIVE TISSUE

A. Fibroblast

The single progenitor of connective tissue; can secrete collagen and elastin (adipocytes, chondrocytes, osteocytes)

B. Connective tissue

Different from other tissues because of large extracellular matrix to cell ratio